In order to investigate the clinical significance of exercise-induced ST changes in patients with prior myocardial infarction, we performed an exercise tolerance test using bicycle ergometer, coronary arteriography and left ventriculography in 77 patients with prior myocardial infarction and compared exercise-induced ST changes with coronary arteriographic and left ventriculographic findings. At end-point time in the exercise test, we observed abnormal ST elevation in 36 patients (46.7%), ST depression in 11 (14.3%) and no significant ST changes in the remaining 30 (39.0%). After exercise, 29 out of 48 patients (60.4%) with prior anterior myocardial infarction had significant ST elevation, 9 (18.8%) had ST depression, and 10 patients (20.8%) had no significant ST changes. Of the 29 patients with exercise-induced ST elevation, 26 (89.6%) had no significant coronary lesion or simply had single vessel disease, and 6 of 9 patients with ST depression (66.7%) had multiple vessel disease. Furthermore, 18 of 29 patients with exercise-induced ST elevation (62.1%) had dyskinesis, 8 (27.6%) had akinsesis and only 3 (10.3%) had hypokinesis. On the other hand, only 2 of 9 patients with exercise-induced ST depression (22.2%) had dyskinesis, 5 had akinesis, and 2 had hypokinesis. Only 7 out of 29 patients (24.1%) with prior inferior myocardial infarction had ST elevation, 2 (6.9%) had ST depression, and no significant ST changes were observed in the remaining 20 (69.0%). No significant correlation was obtained between exercise-induced ST changes and coronary arteriographic and left ventriculographic findings. These findings strongly suggest that exercise-induced ST elevation is commonly observed in patients with anterior myocardial infarction and correlated with the severity of abnormal left ventricular wall movement, and ST depression is related with the extent of coronary artery lesion.

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By means of intracardiac recordings and programmed electrical stimulation of the heart, the combination effect of verapamil and disopyramide on induction of circus movement tachycardia was studied in 8 patients with anomalous extranodal atrioventricular (A-V) pathway. In 4 of 6 patients who manifested reproducible circus movement tachycardia, verapamil, 0.2 mg/kg intravenously administered, prevented the induction of tachycardia by increasing the A-V nodal refractoriness. Disophyramide in a dose of 2 mg/kg was injected 30 minutes after the start of verapamil administration, when prolongation of the A-V nodal conduction time (A-H interval) had continued in most of the patients. Disophyramide lengthened the effective refractory period of the anomalous pathway in all patients in whom this could be determined. The A-H interval which had been prolonged by verapamil, was shortened in 4 patients and almost unchanged in the remaining 4. After addition of disophyramide, sustained tachycardia could be induced in 2 patients who had lost the ability of initiating circus movement tachycardia after verapamil administration. Thus, disophyramide, when administered together with verapamil, may block the effect of verapamil on the A-V node by its anticholinergic action. A concomitant prescription of disopyramide with verapamil in expectation of the depression of both the anomalous pathway and the A-V node may have an untoward outcome.

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The characteristic patterns of the epicardial activation and body surface isopotential maps (MAPs) were examined in experimental transient right bundle branch block (RBBB) produced by pressing the main stem of right bundle mechanically. During the recovery from the complete block, various degrees of incomplete RBBB (IRBBB) were obtained. The epicardial activation of IRBBB spread in almost normal fashion with delayed right ventricular epicardial breakthrough. And the MAPs manifested intermediate patterns between those obtained in control and in complete RBBB (CRBBB). The MAP patterns of IRBBB were classified into the following 3 groups by the difference of the localized bend of isopotential lines reflecting the epicardial breakthrough. In the advanced IRBBB with QRS prolongation over 25%, the epicardial breakthrough of the left ventricle was detected on the MAPs. In the moderate IRBBB with QRS prolongation around 20%, in addition to the left ventricular breakthrough the right ventricular breakthrough was detected at the center of the anterior chest. In the mild IRBBB with QRS prolongation less than 15%, only the right ventricular breakthrough was detected. These findings indicate usefulness of MAPs for diagnosing the severity of IRBBB due to the damage to the main right bundle. Moreover, these MAP patterns in IRBBB of main right bundle can be distinctly differentiated from the IRBBB MAPs resulting from incisional interruption of lateral branches of right bundle. The present findings also suggest the usefulness of MAPs in diagnosing the site of the conduction disturbance resulting in IRBBB.

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To determine the therapeutic effects of glucose-insulin-potassium (GIK) solution, 5 control dogs and 5 GIK-treated dogs were investigated 24 hours after coronary artery occlusion by use of myocardial creatine phosphokinase (CK) activity and myocardial thallium-201 uptake. There was no significant difference in myocardial blood flow estimated by thallium-201 uptake between the control and the GIK group, but myocardial CK activity in the ischemic zone of GIK-treated animals was significantly higher than that of the control group. This suggests that administration of GIK solution is effective in protecting myocardial tissue in the central ischemic area and that this protecting action of GIK seems to be independent of myocardial blood flow.

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A 32-year-old woman of Fanconi syndrome with disorders of amino acid, glucose, uric acid and phosphate reabsorption system in proximal tubule and of renal acid excretion mechanism in distal tubule was reported. By the ammonium chloride loading test, urinary pH could only be decreased by 5.9, and excretion rates of NH⁺₄ and titratable acids were 18.9 and 31.1 mEq/min, respectively. IN the bicarbonate loading test, net renal reabsorption of bicarbonate was 2.96 mEq/100 ml GFR when plasma bicarbonate concentration was 29 mEq/L, and threshold of bicarbonate excretion was 24-26 mEq/L. These results suggest that hydrogen ion excretion disorder in distal tubules exists, while bicarbonate reabsorption ability in proximal tubule is normal.

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The epicardial breakthrough can be recognized from the localized depression of the body surface potential, which is characterized by a localized bend of the equipotential lines or a second-minimum on isopotential maps. Recognition of epicardial breakthrough with isopotential maps enables us to diagnose location of the block site of the bundle branch blocks more precisely than by ECG or VCG. However, the optimum inter-electrode distance for detection of such a localized potential has not been determined. In the present study, influence of the inter-electrode distance on the characteristic patterns reflecting the epicardial breakthrough was studied on 16 healthy persons using 9×9 electrode arrays with inter-electrode distance of 1.25 cm, 5×5 with 2.5 cm, and 3×3 with 5 cm. Breakthrough was recognized in 15 out of 16 cases (94%) on maps recorded with electrode arrays with inter-electrode distance of 1.25 and 2.5 cm. However, detectability of the breakthrough was reduced to 10 out of 16 cases (63%) with electrode array having inter-electrode distance of 5 cm. In conclusion, it is preferable to use an electrode array with an inter-electrode distance of no more than 2.5 cm for the purpose of breakthrough recognition.

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As the processed maps, the variance map and the residue which was the ratio of the nondipolar cardiac field were introduced. The variance map was made from the root mean square of the distance from the mean value of QRS, T or QRST. The variance map may be useful to find the area of the peak variation of QRS, T or QRST on the body surface. The residue is the expression how much was the nondipolar component included in the body surface potentials. This may be relevant to detect the abnormal cardiac potentials included in the body surface potentials.

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To determine the more exact site of origin of ventricular premature beats (VPBs), body surface maps were recorded in 28 patients, aged 15 to 71 years (mean 52) with no cardiac disorders. The site of origin of VPBs was determined from 1) sequential isopotential maps, 2) ventricular activation time (VAT) map and 3) on the basis of maps during pacemaker stimulation at different ventricular areas. To get a three dimensional idea regarding the progression of the ventricular activation front, zero plane was constructed in the human torso by supposing the plane which includes zero potential line on body surface at each instance of ventricular activation. Unipolar lead electrocardiograms were recorded from 85 lead points over the body surface to obtain maps. The site of origin was determined to be from right ventricle 15 patients, from top of interventricular septum in 10 patients, and from left ventricle in 3 patients. Of 15 patients with right ventricular premeture beats, 3 were from outflow region, r were from posterobasal region, 6 were from inflow region and 2 were from apical region. Of 3 patients with left ventricular premature beats, 2 were from posterobasal region and 1 was from high lateral region.

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To investigate the effect of ventricular hypertrophy on the conduction velocity, the transmural conduction velocity was obtained from the findings of echocardiographic and body surface potential mapping examinations on 20 RBBB patients. The transmural conduction velocity was linearly correlated with the ventricular septal thickness and the greater the thickness, the faster was the conduction velocity. There was no statistically significant difference in the duration of the left ventricular activation obtained from the mapping examinations as well as in the time of onset of intrinsicoid deflection i V₅ between the group of left ventricular hypertrophy and that of non-hypertrophy. There was a good linear correlation between the imaginary distance covered by the activation front which proceeded in the direction from endocardium to epicardium during the left ventricular activation and the ventricular septal thickness. These findings were explicable from the faster conduction velocity in the hypertrophied ventricle. The increase in the conduction velocity in the hypertrophy group would be due to cable characteristics of hypertrophied cardiac cells and also due to increase in the number of multiple intercalated discs in the hypertrophied ventricle. It was concluded that the conduction velocity would be an important information to interpret the ECGs in ventricular hypertrophy as well as to estimate the pathological state of the heart.

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Body surface maps were recorded in 26 patients with Wolff-Parkinson-White syndrome, who underwent successful localization and interruption of the accessory conduction pathway. Five types of body surface maps were classified according to the location of the potential maximum and minimum in the delta wave. These 5 types were left free wall type, left posterior septal type, right posterior septal type, right, anterior septal type and right free wall type. Each type correlated well with the location of the accessory pathway, which was determined intraoperatively through epicardial and/or endocardial maps or surgical interruption. The potential minimum zone at 40 msec after the onset of the delta wave appeared at limited areas on the body surface, and this zone was divided into 7 areas which correspond to the location of the accessory pathway.

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1) Body surface mapping was performed in 15 patients with ischemic heart diseade and 5 control subjects before and after isoproterenol infusion. In ischemic heart disease, ST map developed negative areas in the left anterior chest wall extending from mid line to left axillar line after isoproterenol. This distribution on ST depression was different from that of left ventricular hypertrophy or complete left bundle branch block which spared mid anterior chest. The point of maximal ST depression corresponded to one of the conventional chest lead in 6 of 15 cases. In other 9 cases, the point of maximal ST dpression was mostly located superiorly to V₃-V₅. ΣST depression correlated well with the maximal ST depression (r = 0.90) but not very well with ST depression at V₅ (r = 0.70). On ²⁰¹Tl stress scan, a reversible large perfusion defect was detected in 2 out of 5 patients with marked ST depression. These findings suggested that isoproterenol induced ST map changes are useful in diagnosis of myocardial ischemia. 2) Body surface map was obtained in 16 cases with chronic pulmonary disease. The location of the maximum R and initial R was relatively inferior to that of normal controls. Relatively deep S waves were frequently observed. Pulmonary function tests correlated with the maximum R voltage but not with the deepest S. Cases with relatively high pulmonary conus voltage were proved to have right ventricular hypertrophy on ²⁰¹Tl myocardial scintigraphy or on echocardiography.

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To locate the ischemic area in 22 patients with angina pectoris, exercise stress body surface isopotential maps (MAPs) were assessed and compared with coronary angiography and myocardial stress scintigraphy. Taking coronary angiographic findings into consideration, 4 types of ischemic MAP responses, i.e., septum and anterior, lateral, inferior, and posterior wall ischemia were postulated. Sensitivity of stress MAP was 71% for the average and more than stress imaging. Specificity of stress MAP was 46% for the average and less than stress imaging.

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Using the ST difference map after the treadmill exercise test, the 26 patients with coronary artery disease were studied. 1) The extent and the speed of complete recovery of ST depression or negative area were well correlated with the severity of coronary artery disease. 2) ST elevation or positive area was correlated with regional asynergies. 3) ST elevation area disclosed regional defect ²⁰¹Tl scintigram at rest, while ST depression area could disclose it infrequently.

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For the quantitative assessment of infarct site and size in patients with acute myocardial infarction, an attempt was made to solve the inverse problem, that is, to characterize ST vector in the infarcted myocardium from ST segment deviations in 39 precordial leads and their sterical positions A simple inverse model was employed, assuming that the source origin of ST segment displacement in surface electrocardiograms was a single unfixed dipole embedded in the homogeneous infinite medium. The magnitude, direction and position of ST vector were calculated as an inverse solution by computer. The direction of ST vector determined by this inverse problem was well in accord with infarct site assessed by left ventriculography or myocardial scintigraphy carried out later. However, the magnitude of ST vector was poorly correlated (r = 0.47, p<0.05, n = 17) with infarct size estimated from serum creatine phosphokinase, although a good correlation ( r = 0.74) was obtained when 3 cases with extremely large infarction were excluded. These results suggest that our inverse solution of ST vector is useful for prediction of the site and size of acute myocardial infarction.

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